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Exercise and Parkinson’s Neural Mitochondria
Treadmill training attenuated complex I deficits, cytochrome c release, ATP depletion, and complexes II–V abnormalities in Parkinson’s disease. Studies analyzed the neural mitochondrial quality-control, reporting that treadmill exercise improved mitochondrial biogenesis, mitochondrial fusion, and mitophagy in Parkinson’s disease. The hypothesis that treadmill training could attenuate both neural mitochondrial respiratory deficiency and neural mitochondrial quality-control dysregulation in Parkinson’s disease, suggesting that treadmill training might slow down the progression of Parkinson’s disease.
2. Treadmill Exercise on Neural Mitochondrial Functions in Parkinson’s Disease
2.1. Effects of TE Training on Neural Mitochondrial Respiratory Deficiency in PD
2.2. Effects of TE Training on Neural Mitochondrial Biogenesis in PD
2.3. Effects of TE Training on Neural Mitochondrial Dynamics in PD
2.4. Effects of TE Training on Neural Mitophagy in PD
(1) Treadmill training attenuated neural mitochondrial respiratory deficiency in Parkinson’s disease, supported by the evidence that treadmill training normalized the levels of complexes I–V, cytochrome c, and ATP production in the Parkinsonian brain. (2) Treadmill training optimized neural mitochondrial biogenesis in Parkinson’s disease, supported by the evidence that treadmill training increased or normalized the levels of biogenesis regulators (SIRT3, SIRT1, AMPK, PGC-1α, NRF-1,2, and TFAM) and import machinery (TOM-20, TOM-40, TIM-23, and mtHSP70) in the Parkinsonian brain. (3) Treadmill training enhanced the neural mitochondrial fusion in Parkinson’s disease, supported by the evidence that treadmill training increased mitochondrial fusion factors (OPA-1 and MFN-2) in the Parkinsonian brain. (4) Treadmill training repaired the impairment of mitophagy in Parkinson’s disease, supported by the evidence that treadmill training reduced the levels of dysfunctional mitochondria detectors (PINK1, parkin, and p62) and increased the levels of lysosomal factors (LAMP2 and cathepsin L) in the Parkinsonian brain. Taking these findings with the previously hypothesized pathophysiology of Parkinson’s disease together, we drew a hypothesized figure (Figure 1), which suggests that treadmill training could counteract the neurodegeneration of Parkinson’s disease in both the neural mitochondrial respiratory system and neural mitochondrial quality-control.
4. The Implications for Future Research
Further interdisciplinary studies are required to investigate the effects of treadmill training on the neural mitochondrial respiratory system, biogenesis, dynamics, and mitophagy in both genetic models and toxin models of Parkinson’s disease. Additionally, clinical studies should clarify the possible therapeutic applications through different exercise interventions into neural mitochondrial dysfunction in Parkinson’s disease.
The entry is from 10.3390/biomedicines9081011
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